Niedomykalność zastawki aortalnej
Patofizjologia i mechanizm
Niedomykalność zastawki aortalnej (NZA) charakteryzuje się wstecznym przepływem krwi z aorty do lewej komory podczas rozkurczu, co prowadzi do przeciążenia objętościowego i ciśnieniowego serca. Etiologia obejmuje pierwotne zmiany płatków zastawki (np. zastawka dwupłatkowa, infekcyjne zapalenie wsierdzia) oraz wtórne zmiany korzenia aorty (np. poszerzenie aorty, choroby tkanki łącznej). Patofizjologia różni się w zależności od ostrego lub przewlekłego przebiegu: ostra NZA powoduje gwałtowny wzrost ciśnienia końcoworozkurczowego lewej komory i ryzyko obrzęku płuc, natomiast przewlekła NZA prowadzi do adaptacyjnego powiększenia i przerostu lewej komory, z czasem skutkując dysfunkcją skurczową i spadkiem frakcji wyrzutowej. Charakterystyczne zmiany hemodynamiczne obejmują zwiększenie objętości końcoworozkurczowej i ciśnienia tętna aorty, a także zmiany w pętli ciśnienie-objętość lewej komory, co wpływa na przebieg kliniczny i rokowanie.
- Niedomykalność zastawki aortalnej – patogeneza i mechanizm
- Podstawowe mechanizmy niedomykalności zastawki aortalnej
- Patofizjologia na poziomie komórkowym
- Rola macierzy pozakomórkowej
- Różnice między ostrą i przewlekłą niedomykalnością zastawki aortalnej
- Mechanizmy objawów i kompensacji
- Przyczyny niedomykalności zastawki aortalnej
- Mechanizmy hemodynamiczne
- Adaptacja i remodeling serca
- Implikacje kliniczne i terapeutyczne
Niedomykalność zastawki aortalnej – patogeneza i mechanizm
Niedomykalność zastawki aortalnej (NZA) to stan, w którym zastawka aortalna nie zamyka się całkowicie, powodując wsteczny przepływ krwi z aorty do lewej komory serca podczas rozkurczu. Patofizjologia tego schorzenia jest złożona i zależy od wielu czynników, w tym od mechanizmu nieprawidłowego zamykania się płatków zastawki oraz od tempa rozwoju choroby.12
Podstawowe mechanizmy niedomykalności zastawki aortalnej
Niedomykalność zastawki aortalnej jest spowodowana nieprawidłowym zamykaniem się (malkoaptacją) płatków zastawki aortalnej, co może wynikać z:12
- Wewnętrznych nieprawidłowości samej zastawki (pierwotna NZA)
- Poszerzenia lub geometrycznego zniekształcenia korzenia aorty (wtórna NZA)
- Kombinacji obu powyższych mechanizmów
Klasyfikacja funkcjonalna według El Khoury opisuje różne typy niedomykalności aortalnej:123
- Typ I – związany z poszerzeniem funkcjonalnego pierścienia aortalnego, przy normalnym ruchu płatków
- Typ II – związany z nadmiernym ruchem płatków (wypadanie)
- Typ III – związany z ograniczonym ruchem płatków
Patofizjologia na poziomie komórkowym
Na poziomie komórkowym zastawka aortalna składa się z komórek śródbłonka zastawkowego (VECs) oraz komórek śródmiąższowych zastawki (VICs), osadzonych w złożonej sieci macierzy pozakomórkowej (ECM). Dynamiczne środowisko zastawki aortalnej sprawia, że zmiany hemodynamiczne występujące u pacjentów z niedomykalnością zastawki aortalnej mogą znacząco przyczyniać się do progresji choroby, nawet u pacjentów bezobjawowych.1
Zmiany hemodynamiczne prowadzą do przebudowy zastawki aortalnej poprzez współdziałanie między ścieżkami sygnałowymi na poziomie molekularnym, komórkowym i strukturalnym. Na poziomie molekularnym zastawka aortalna zawiera różne rodziny białek regulujących i utrzymujących strukturę i funkcję zastawki, głównie poprzez interakcje z macierzą pozakomórkową.1
Rola macierzy pozakomórkowej
Macierz pozakomórkowa jest ważnym regulatorem funkcji komórek i tkanek. Zorganizowana zastawkowa ECM tworzy płatki zastawki i zawiera trzy nakładające się warstwy, każda o odmiennych właściwościach: ventricularis, spongiosa i fibrosa. Zmiany w ECM są centralnym elementem sieci, z której następuje przebudowa zastawki.1
Istotne elementy w przebudowie ECM i regulacji zastawki to:1
- Kwas hialuronowy, stanowiący 60% całkowitej zawartości glikozaminoglikanów (GAG) w sercu
- Białka macierzy międzykomórkowej
- Rodzina transformującego czynnika wzrostu beta (TGF-β), która ma kluczową rolę w organizacji ECM
Wszelkie zaburzenia w tych ścieżkach sygnałowych mogą prowadzić do nieprawidłowości zastawki aortalnej i przyczyniać się do rozwoju niedomykalności.12
Różnice między ostrą i przewlekłą niedomykalnością zastawki aortalnej
Patofizjologia niedomykalności zastawki aortalnej zależy od tego, czy jest ona ostra czy przewlekła. Różnice w mechanizmach i konsekwencjach są znaczące.1
Ostra niedomykalność zastawki aortalnej
W ostrej niedomykalności zastawki aortalnej o znacznym nasileniu dochodzi do nagłego zwiększenia objętości krwi w lewej komorze podczas rozkurczu. Lewa komora nie ma wystarczająco dużo czasu, aby rozszerzyć się w odpowiedzi na nagły wzrost objętości. W rezultacie:12
- Ciśnienie końcoworozkurczowe w lewej komorze gwałtownie wzrasta
- Zwiększa się ciśnienie w żyłach płucnych
- Zmienia się dynamika przepływu wieńcowego
- Może szybko rozwinąć się obrzęk płuc i wstrząs kardiogenny
Nagły początek ciężkiej niedomykalności aortalnej jest zwykle stanem zagrożenia życia wymagającym natychmiastowej interwencji chirurgicznej, ponieważ lewa komora nie jest w stanie szybko zaadaptować się do nagłego wzrostu objętości końcoworozkurczowej spowodowanego wstecznym przepływem.1
Przewlekła niedomykalność zastawki aortalnej
W przewlekłej niedomykalności zastawki aortalnej lewa komora przechodzi szereg zmian adaptacyjnych:1
- Powiększenie lewej komory
- Ekscentryczny przerost mięśnia sercowego
- Dodanie sarkomerów w serii (powodujące dłuższe włókna mięśniowe)
- Reorganizacja włókien mięśniowych
Te adaptacyjne mechanizmy pozwalają lewej komorze funkcjonować jako wydajną pompę o wysokiej podatności, obsługującą dużą objętość wyrzutową, często z niewielkim wzrostem ciśnienia napełniania. Podczas wysiłku opór naczyń obwodowych spada, a przy wzroście częstości akcji serca skraca się rozkurcz, co zmniejsza niedomykalność na cykl i ułatwia zwiększenie efektywnej (do przodu) pojemności minutowej bez znacznego zwiększenia objętości i ciśnienia końcoworozkurczowego.12
Z czasem jednak lewa komora osiąga swoją maksymalną średnicę i ciśnienie rozkurczowe zaczyna wzrastać, powodując objawy (duszność), które mogą nasilać się podczas wysiłku. Rosnące ciśnienie końcoworozkurczowe w lewej komorze może również obniżać gradienty perfuzji wieńcowej, powodując niedokrwienie podwsierdziowe i mięśnia sercowego, martwicę i apoptozę.1
Mechanizmy objawów i kompensacji
Przeciążenie objętościowe i ciśnieniowe
Niedomykalność zastawki aortalnej powoduje zarówno przeciążenie objętościowe (podwyższony preload), jak i przeciążenie ciśnieniowe (podwyższony afterload) serca:12
- Wsteczny przepływ krwi do lewej komory powoduje przeciążenie objętościowe i wzrost preloadu
- Przeciążenie ciśnieniowe powoduje przerost lewej komory (LVH)
- W niedomykalności aortalnej występuje zarówno przerost koncentryczny, jak i ekscentryczny
W skompensowanej niedomykalności aortalnej dochodzi do wystarczającego pogrubienia ściany lewej komory, dzięki czemu stosunek grubości ściany do promienia jamy pozostaje prawidłowy. W tych warunkach końcoworozkurczowy stres ściany utrzymuje się na normalnym poziomie lub wraca do normy.12
Dekompensacja i niewydolność lewej komory
W miarę utrzymywania się i nasilania niedomykalności aortalnej, pogrubienie ściany nie nadąża za obciążeniem hemodynamicznym i rośnie końcowoskurczowy stres ściany. W tym momencie niedopasowanie obciążenia następczego powoduje spadek funkcji skurczowej, a frakcja wyrzutowa spada.12
W przewlekłej zdekompensowanej niedomykalności aortalnej upośledzone opróżnianie lewej komory prowadzi do zwiększenia objętości końcowoskurczowej i spadku frakcji wyrzutowej (EF), całkowitej objętości wyrzutowej i objętości wyrzutowej do przodu. Dochodzi do dalszego poszerzenia serca i ponownego wzrostu ciśnienia napełniania lewej komory.1
Bezpośrednio po wymianie zastawki preload szacowany przez EDV (objętość końcoworozkurczowa) zmniejsza się, podobnie jak ciśnienie napełniania. ESV (objętość końcowoskurczowa) również się zmniejsza, ale w mniejszym stopniu. Efektem jest początkowy spadek frakcji wyrzutowej. Pomimo tych zmian, wyeliminowanie niedomykalności prowadzi do zwiększenia objętości wyrzutowej do przodu, a z czasem frakcji wyrzutowej.1234
Przyczyny niedomykalności zastawki aortalnej
Niedomykalność zastawki aortalnej może być spowodowana różnymi stanami wpływającymi na zastawkę aortalną, korzeń aorty lub kombinacją obu.1
Pierwotne przyczyny uszkodzenia zastawki
Pierwotna niedomykalność aortalna wynika z wewnętrznych nieprawidłowości płatków zastawki:12
- Zastawka dwupłatkowa aortalna (najczęstsza wrodzona wada serca, związana z niedomykalnością w 20-70% przypadków)
- Choroby zwyrodnieniowe (zwapnienie, włóknienie)
- Infekcyjne zapalenie wsierdzia (aktywne lub wygojone)
- Gorączka reumatyczna
- Uszkodzenie płatków indukowane lekami (fenfluramine, phentermine)
Wtórne przyczyny uszkodzenia aorty
Wtórna niedomykalność aortalna występuje, gdy płatki zastawki aortalnej wydają się strukturalnie prawidłowe, ale nie domykają się z powodu patologii korzenia aorty:12
- Idiopatyczne poszerzenie aorty
- Poszerzenie aorty związane z nadciśnieniem
- Układowe choroby tkanki łącznej (choroba reumatyczna, reumatoidalne zapalenie stawów)
- Poszerzenie lub rozwarstwienie aorty wstępującej
- Aortopatia związana z zastawką dwupłatkową
- Kiłowe choroby aorty
Choroby tkanki łącznej, takie jak zespół Marfana, zespół Loeysa-Dietza i naczyniowy zespół Ehlersa-Danlosa, często prowadzą do wtórnej niedomykalności aortalnej z powodu aortopatii.1
Rzadsze przyczyny
Inne, rzadsze przyczyny niedomykalności zastawki aortalnej obejmują:1
- Rozdarcie lub uraz głównej tętnicy ciała (aorty)
- Uraz klatki piersiowej
- Rozwarstwienie aorty (rozdarcie wewnętrznej warstwy aorty)
- Choroby układu immunologicznego, takie jak toczeń
Mechanizmy hemodynamiczne
Hemodynamiczne konsekwencje niedomykalności zastawki aortalnej są złożone i wpływają na funkcjonowanie całego układu krążenia.1
Zmiany ciśnienia i objętości
W niedomykalności aortalnej występują charakterystyczne zmiany ciśnienia i objętości:1
- Ponieważ komora jest napełniana z dwóch źródeł (aorty i lewego przedsionka), prowadzi to do znacznie większego napełniania lewej komory
- Objętość końcoworozkurczowa lewej komory wzrasta, co zwiększa ciśnienie końcoworozkurczowe lewej komory
- Charakterystyczną cechą niedomykalności aortalnej jest zwiększenie ciśnienia tętna aorty (ciśnienie skurczowe minus rozkurczowe)
Podwyższone ciśnienie końcoworozkurczowe lewej komory powoduje cofanie się krwi do lewego przedsionka i żył płucnych, co zwiększa ciśnienie w lewym przedsionku i ciśnienie zaklinowania w kapilarach płucnych, mogąc powodować przekrwienie płuc i obrzęk.1
Pętla ciśnienie-objętość
W niedomykalności zastawki aortalnej występują charakterystyczne zmiany w pętli ciśnienie-objętość lewej komory:1
- Zastawka aortalna nie zamyka się całkowicie po zakończeniu wyrzutu skurczowego
- Gdy komora rozluźnia się podczas rozkurczu, krew przepływa z aorty z powrotem do komory
- Brak prawdziwej fazy izowolumetrycznego rozluźnienia (brak pionowej linii między zamknięciem zastawki aortalnej a otwarciem zastawki mitralnej)
- Po otwarciu zastawki mitralnej napełnianie następuje z lewego przedsionka, ale krew nadal wpływa z aorty do komory przez cały rozkurcz
Zwiększona objętość końcoworozkurczowa (zwiększony preload) aktywuje mechanizm Franka-Starlinga, zwiększając siłę skurczu, szczytowe ciśnienie komorowe (skurczowe) i objętość wyrzutową (co widać po zwiększonej szerokości pętli ciśnienie-objętość).1
Adaptacja i remodeling serca
Remodeling serca w odpowiedzi na niedomykalność aortalną jest kluczowym elementem patofizjologii i determinuje przebieg kliniczny.1
Mechanizmy kompensacyjne
W przewlekłej niedomykalności aortalnej lewa komora adaptuje się do przeciążenia objętościowego poprzez serię mechanizmów kompensacyjnych:1
- Zwiększenie objętości końcoworozkurczowej
- Zwiększenie podatności komory, które dostosowuje zwiększoną objętość bez wzrostu ciśnienia napełniania
- Kombinacja przerostu ekscentrycznego i koncentrycznego
Wraz z postępem choroby, rekrutacja rezerwy preload i kompensacyjny przerost pozwalają lewej komorze utrzymać prawidłową funkcję wyrzutową pomimo podwyższonego afterloadu.1
Przebudowa lewej komory
Z czasem, przy długotrwałym przeciążeniu objętościowym, lewa komora ulega dramatycznym zmianom:1
- Zwiększa się objętość końcoworozkurczowa i końcowoskurczowa
- Rozwija się przerost ekscentryczny i koncentryczny
- Komora przyjmuje bardziej sferyczny kształt
Dramatyczne powiększenie serca, obserwowane w niedomykalności aortalnej, nazywane jest „cor bovinum”. Uważa się, że „niedomykalność aortalna powoduje niedomykalność aortalną” – wysoki oscylacyjny przepływ związany z niedomykalnością aortalną może prowadzić do dalszego poszerzenia aorty, co z kolei może prowadzić do dalszego pogorszenia niedomykalności aortalnej.1
Dysfunkcja skręczowa lewej komory
Dysfunkcja skurczowa lewej komory (definiowana jako frakcja wyrzutowa poniżej normy w spoczynku) jest początkowo odwracalnym zjawiskiem związanym głównie z nadmiernym obciążeniem następczym, a po wymianie zastawki aortalnej możliwe jest pełne przywrócenie wielkości i funkcji lewej komory.1
Z czasem, gdy lewa komora rozwija postępujące powiększenie komory i bardziej sferyczną geometrię, obniżona kurczliwość mięśnia sercowego zaczyna dominować nad nadmiernym obciążeniem jako przyczyna postępującej dysfunkcji. Szereg badań wykazało, że funkcja skurczowa lewej komory i wielkość końcowoskurczowa są najważniejszymi determinantami przeżycia i pooperacyjnego powrotu funkcji lewej komory u pacjentów poddawanych wymianie zastawki z powodu przewlekłej niedomykalności aortalnej.1
Implikacje kliniczne i terapeutyczne
Zrozumienie patofizjologii niedomykalności zastawki aortalnej ma kluczowe znaczenie dla podejmowania decyzji klinicznych i terapeutycznych.1
Diagnostyka i monitorowanie
Echokardiografia jest podstawowym narzędziem do diagnozy i oceny ilościowej stopnia niedomykalności aortalnej, a także do określenia etiologii i mechanizmu niewydolności zastawki.1
Klasyfikacja funkcjonalna jest nieocenionym narzędziem, które pomaga klinicystom systematycznie oceniać zachowanie zastawki i może wpływać na rodzaj wybranej interwencji dla zastawki.1
W ocenie ilościowej niedomykalności aortalnej:1
- VC (vena contracta) reprezentuje najmniejszą średnicę przepływu strumienia niedomykalności przepływającego przez zastawkę aortalną
- EROA ≥0,30 cm², objętość fali zwrotnej ≥60 ml i frakcja niedomykalności ≥50% wskazują na ciężką niedomykalność aortalną
Leczenie farmakologiczne i chirurgiczne
Obniżenie obciążenia następczego (opór obwodowy) stało się podstawą farmakoterapii w niedomykalności aortalnej. Wszystkie inne czynniki będące równe, zwiększony opór obwodowy będzie związany ze zwiększoną niedomykalnością.1
W przypadku ostrej niedomykalności aortalnej o ciężkim nasileniu najczęściej zalecana jest natychmiastowa interwencja chirurgiczna. W niektórych przypadkach przez krótki okres można stosować leki w celu stymulacji serca lub rozszerzenia lub zwężenia naczyń krwionośnych.1
W przewlekłej ciężkiej niedomykalności aortalnej, chirurgia jest często zalecana. Czas operacji jest ważny do omówienia z lekarzem i chirurgiem. W niektórych przypadkach ciężka niedomykalność aortalna może być leczona farmakologicznie. Leki mogą być również stosowane krótkoterminowo przed operacją wymiany zastawki lub na bieżąco, jeśli pacjent nie jest w stanie poddać się operacji wymiany zastawki.1
Nowe podejścia terapeutyczne
Pacjenci w Południowej Karolinie z ciężką niedomykalnością aortalną wcześniej mieli tylko jedną opcję leczenia: operację na otwartym sercu. Jednak dzięki nowej technologii zastawek serca przezcewnikowych, nowa zastawka aortalna może być umieszczona w chorej zastawce za pomocą już ustalonej, minimalnie inwazyjnej techniki znanej jako przezcewnikowa wymiana zastawki aortalnej (TAVR).1
Ta metoda okazała się skuteczna w leczeniu stenozy aortalnej, czyli zwężenia zastawki ograniczającego przepływ krwi, ale nie była stosowana do leczenia niedomykalności aortalnej do tej pory. Dzięki temu urządzeniu lekarze mogą umieścić zdrową zastawkę wewnątrz przeciekającej, przypinając ją do oryginalnych płatków naturalnej zastawki bez użycia szwów.1
To nowe urządzenie umożliwia TAVR większej liczbie pacjentów. Urządzenie dostosowuje się do naturalnej anatomii pacjenta, co umożliwia lepszy i bardziej efektywny przepływ krwi do tętnic serca.1
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Materiały źródłowe
- #1 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVRhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7288848/
Aortic insufficiency (AI) or regurgitation is caused by the malcoaptation of the aortic valve (AV) cusps due to intrinsic abnormalities of the valve itself, a dilatation or geometric distortion of the aortic root, or by some combination thereof. […] Recent close examination of such pathological processes has demonstrated a wide array of complex, active remodeling mechanisms affecting the valve and surrounding structures. […] New and ongoing research into the pathophysiology underlying these remodeling mechanisms has facilitated important discoveries pertaining to preventative, diagnostic, and mitigating strategies for patients with AI. […] This review will aim to describe various mechanisms involved in AI development, dissect some of the cross-talk among known and possible signaling pathways leading to valve remodeling, identify an association between these pathways and possible pharmacological approaches, and discuss surgical implications for management of these pathological processes.
- #1 Chronic aortic regurgitation: diagnosis and therapy in the modern erahttps://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/chronic-aortic-regurgitation-diagnosis-and-therapy-in-the-modern-era
Aortic regurgitation (AR) is a complex and multifactorial valvular disease. […] Aortic regurgitation (AR, also termed aortic insufficiency) results in diastolic blood flow from the aorta back into the left ventricle (LV) and may be caused by a variety of acquired or congenital aetiologies preventing complete coaptation of the aortic valve (AV) leaflets (also called cusps). Primary (organic) AR is an intrinsic disease of the AV leaflets, whereas secondary (functional) AR results from distortion or dilation of the aortic root and/or ascending aorta leading to incomplete aortic leaflet coaptation. […] Some disease entities may cause AR by both mechanisms. For example, Marfans syndrome and bicuspid aortic valve (BAV) pathologies do affect the structure of the AV and may also cause dilatation of the aortic root and ascending aorta leading to a functionally regurgitant valve. Endocarditis may cause valve destruction by erosion of the leaflet edges or leaflet perforation.
- #1 Functional and pathomorphological anatomy of the aortic valve and root for aortic valve sparing surgery in tricuspid and bicuspid aortic valves – Jahanyar- Annals of Cardiothoracic Surgeryhttps://www.annalscts.com/article/view/17021/html
The aortic valve (AV) is a three-dimensional structure, with leaflets that are suspended within the functional aortic annulus (FAA). These structures (AV and FAA) are therefore intrinsically connected and disease of just one component can independently lead to AV dysfunction. Hence, AV dysfunction can occur in the setting of entirely normal valve leaflets. However, as these structures are functionally inter-connected, disease of one component can lead to abnormalities of the other over time. Thus, AV dysfunction is often multifactorial. […] Loss of integrity of any of these components leads to AV dysfunction, regurgitation or even stenosis. Moreover, based on the principles of the mechanism of mitral regurgitation set forth by Alain Carpentier, Gebrine El Khoury has developed the functional classification for aortic regurgitation (AR) during the late 90s and early into the new millennium.
- #1 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVRhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7288848/
On a cellular level, the AV is comprised of valvular interstitial cells (VICs) and valvular endothelial cells (VECs), both of which are seeded within intricate, interactive networks of extracellular matrices. […] Considering the dynamic microenvironment present within the AV, the hemodynamic changes demonstrated in patients with AI can contribute strongly to the progression of the disease, even in the setting of an asymptomatic patient. […] Ultimately, these hemodynamic changes to the local environment can then lead to further remodeling in the AV through an interplay between molecular, cellular, and structural signaling pathways. […] At the molecular level, the AV contains various protein families that regulate and maintain valve structure and function, primarily through interactions with the extracellular matrix (ECM).
- #1 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVRhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7288848/
The ECM is an important regulator of cell and tissue function and may be defined as the diverse collection of proteins and sugars that surrounds cells in all solid tissues. […] The organized valvular ECM makes up the cusps of the valve and contains three overlapping layers, each with distinct properties: the ventricularis, the spongiosa, and the fibrosa. […] Given the highly interconnected network of proteins and pathways involved in ECM maintenance that have been implicated in AI development, it is safe to suggest that the ECM changes are at the center of the network from which valve remodeling occurs. […] Cardiac remodeling resulting in AI can manifest itself in various ways, such as prolapse, degeneration, and calcification, which can result in changes in the hemodynamic properties of the valve. […] The rise of proteomics and knockout studies on individual proteins in mice over recent years has demonstrated that numerous different proteins can contribute to AV remodeling and AI when inactivated.
- #1 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVRhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7288848/
Hyaluronan, a glycosaminoglycan (GAG), constitutes 60% of the total GAG content in the heart and carries out various functions including cell interactions and linking proteins with aggrecan, making it an important component of the valvular ECM. […] Another family of proteins implicated in AV remodeling and regulation are matricellular proteins. […] In the regulation of the AV structure, the transforming growth factor beta (TGF-) superfamily is one of the largest molecular components. […] Given TGF-s important role in ECM organization, any valvular remodeling will likely be associated with altered TGF- expression, thereby directly impacting the molecular structure of the AV. […] As aforementioned, a major protein with significant impact on the ECM is TGF-. […] Given the wide array of genomic and proteomic pathways involved in AV dysregulation, it becomes clear that many more genes and proteins likely contribute to this process as well.
- #1 Aortic Regurgitation: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/150490-overview
The pathophysiology of AR depends on whether the AR is acute or chronic. In acute AR, the LV does not have time to dilate in response to the volume load, whereas in chronic AR, the LV may undergo a series of adaptive (and maladaptive) changes. […] Acute AR of significant severity leads to increased blood volume in the LV during diastole. The LV does not have sufficient time to dilate in response to the sudden increase in volume. As a result, LV end-diastolic pressure increases rapidly, causing an increase in pulmonary venous pressure and altering coronary flow dynamics. […] Chronic AR causes gradual left ventricular volume overload that leads to a series of compensatory changes, including LV enlargement and eccentric hypertrophy. LV dilation occurs through the addition of sarcomeres in series (resulting in longer myocardial fibers), as well as through the rearrangement of myocardial fibers.
- #1 Aortic regurgitation pathophysiology – wikidochttps://www.wikidoc.org/index.php/Aortic_regurgitation_pathophysiology
In acute aortic insufficiency, there is a sudden decrease in stroke volume and subsequent increase in left ventricular end diastolic volume thereby causing decrease cardiac output with resultant reflex tachycardia. The sharply rising high left ventricular end diastolic pressure and reflex tachycardia causes profound hypotension and cardiogenic shock. […] In chronic aortic insufficiency, initially the left ventricle remains complaint, thereby compensates for increased left ventricular end diastolic volume by progressive left ventricular dilatation and left ventricular hypertrophy, which maintains normal ratio of wall thickness to the cavity radius, thereby maintaining normal wall stress. Overtime, when the left ventricular hypertrophy fails to keep up with chronic volume overload, end systolic wall stress rises and at this point the left ventricle fails and results in left ventricle decompensation causing reduction in the left ventricular wall compliance with resultant congestive heart failure.
- #1 Acute aortic regurgitation in adults – UpToDatehttps://www.uptodate.com/contents/acute-aortic-regurgitation-in-adults
The acute onset of severe aortic regurgitation (AR, also called aortic insufficiency) is usually a medical emergency due to the inability of the left ventricle to quickly adapt to the abrupt increase in end-diastolic volume caused by the regurgitant flow. If not surgically corrected, acute severe AR commonly results in cardiogenic shock. […] Aortic dissection can result in AR by four mechanisms: dilation of the sinuses with incomplete coaptation of the leaflets at the center of the valve; involvement of a valve commissure resulting in inadequate leaflet support; direct extension of the dissection into the base of a leaflet, resulting in a flail valve leaflet; and prolapse of the dissection flap across the aortic valve into the left ventricular outflow tract in diastole impeding leaflet closure. Patients with a bicuspid aortic valve are at higher risk of aortic dissection.
- #1 6.5: Aortic Regurgitation – Medicine LibreTextshttps://med.libretexts.org/Bookshelves/Medicine/Textbook_of_Cardiology/06%3A_Valvular_Disease/6.05%3A_Aortic_Regurgitation
Aortic root dilatation, annular dilation and congenital bicuspid valve are, in developed countries, the most common causes of severe chronic aortic valve regurgitation. […] The slow process of chronic aortic regurgitation allows adaptation of the ventricle to the increased preload and afterload. […] The left ventricle compensates to the regurgitant flow, the increased volume and pressure by enlargement. […] In contrast to the compensatory mechanism in mitral valve regurgitation, a modest concentric left ventricular hypertrophy accompanies the eccentric hypertrophy, with a normal mass-to-volume ratio. […] In a chronic state, progressive left ventricle dilatation leads to pre- and afterload mismatch.
- #1 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #1 Aortic Regurgitation: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/150490-overview
Eventually, the LV reaches its maximal diameter and diastolic pressure begins to rise, resulting in symptoms (dyspnea) that may worsen during exercise. Increasing LV end-diastolic pressure may also lower coronary perfusion gradients, causing subendocardial and myocardial ischemia, necrosis, and apoptosis.
- #1 Aortic regurgitation – Wikipediahttps://en.wikipedia.org/wiki/Aortic_regurgitation
Aortic regurgitation causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart. […] The volume overload, due to elevated pulse pressure and the systemic effects of neuroendocrine hormones causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular pressure overload associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction. […] Physiologically, in individuals with a normally functioning aortic valve, the valve is only open when the pressure in the left ventricle is higher than the pressure in the aorta. This allows the blood to be ejected from the left ventricle into the aorta during ventricular systole. The amount of blood that is ejected by the heart is known as the stroke volume. Under normal conditions, 50% of the blood in a filled left ventricle is ejected into the aorta to be used by the body. After ventricular systole, the pressure in the left ventricle decreases as it relaxes and begins to fill up with blood from the left atrium. This relaxation of the left ventricle (early ventricular diastole) causes a fall in its pressure. When the pressure in the left ventricle falls below the pressure in the aorta, the aortic valve will close, preventing blood in the aorta from going back into the left ventricle.
- #1 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #1 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #1 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #1 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #1 Aortic valve regurgitation – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/aortic-valve-regurgitation/symptoms-causes/syc-20353129
In aortic valve regurgitation, the aortic valve doesn’t close properly. This causes blood to flow backward from the body’s main artery, called the aorta, into the lower left heart chamber, called the left ventricle. […] Aortic valve regurgitation also called aortic regurgitation is a type of heart valve disease. The valve between the lower left heart chamber and the body’s main artery doesn’t close tightly. As a result, some of the blood pumped out of the heart’s main pumping chamber, called the left ventricle, leaks backward. […] In aortic valve regurgitation, the valve doesn’t close properly. This causes blood to leak back into the lower left heart chamber, called the left ventricle. As a result, the chamber holds more blood. This could cause it to get larger and thicken. […] Any condition that damages the aortic valve can cause aortic valve regurgitation. Causes may include:
- #1 Incidence and Pathology of Aortic Regurgitation | ICR Journalhttps://www.icrjournal.com/articles/incidence-and-pathology-aortic-regurgitation?language_content_entity=en
Aortic regurgitation (AR) can arise from degenerative, congenital, inflammatory and infectious aetiologies, manifesting as primary AR with intrinsic leaflet disease, secondary AR due to aortopathy or annular dilatation, or a combination. […] The aetiology of AR may be diverse, encompassing degenerative (degeneration of aortic root and/or aortic leaflet), congenital, inflammatory and infectious factors. The AR mechanism can be primary with aortic valve leaflet abnormality, secondary with preserved aortic leaflets such as aortic root or annular dilatation, or a combination. […] Aortic valve leaflet degeneration is the dominant cause of primary AR. Primary AR consists of calcific degenerative leaflet disease, commonly associated with AS. […] Other causes of primary AR feature intrinsic leaflet disorders such as leaflet perforation, prolapse, or restriction.
- #1 Incidence and Pathology of Aortic Regurgitation | ICR Journalhttps://www.icrjournal.com/articles/incidence-and-pathology-aortic-regurgitation?language_content_entity=en
In secondary AR, the aortic valve leaflets appear structurally normal. Aortic root pathology with dilatation can create secondary AR through aortic valve leaflet malcoaptation, retraction and prolapse. […] The bicuspid aortic valve phenotype is the most common congenital heart defect, and associated with AR in 20-70% of cases. […] Primary AR can develop due to abnormal shear stress leading to degenerative leaflet thickening, restriction, or prolapse. […] Connective tissue disorders such as Marfan, Loeys-Dietz and vascular Ehlers-Danlos syndromes commonly result in secondary AR due to aortopathy. […] The main cause of acute secondary AR is aortic dissection, which may be iatrogenic or due to the above-mentioned aortopathies. […] In acute AR, the sudden onset of severe diastolic regurgitation results in a rapid increase in LV end diastolic volume and pressure, which may spiral towards pulmonary congestion and cardiogenic shock. In chronic AR, the left ventricle has the time to adapt to the volume overload and the LV end diastolic pressure volume relationship flattens, which postpones the occurrence of symptoms. Remodelling includes LV dilatation, eccentric hypertrophy and increased stroke volume to compensate for the regurgitation volume. However, over time the incessant volume overload will overrule the ventricular compensatory remodelling capacity. Eventually, this cascade will progress to LV dilatation, myocardial fibrosis and systolic failure with depressed LVEF.
- #1 Aortic valve regurgitation – Symptoms and causes – Mayo Clinichttps://www.mayoclinic.org/diseases-conditions/aortic-valve-regurgitation/symptoms-causes/syc-20353129
Other rare conditions can cause the aorta to get bigger and damage the aortic valve. These include a connective tissue disease called Marfan syndrome. Some immune system conditions, such as lupus, also can lead to aortic valve regurgitation. […] Tear or injury of the body’s main artery. The body’s main artery is the aorta. A traumatic chest injury may damage the aorta and cause aortic regurgitation. So might a tear in the inner layer of the aorta, called an aortic dissection.
- #1 CV Physiology | Valvular Insufficiency (Regurgitation)https://cvphysiology.com/heart-disease/hd005
Aortic regurgitation occurs when the aortic valve cannot close completely and blood flows back from the aorta (Ao) into the left ventricle after ejection into the aorta is complete. […] Because the ventricle is being filled from two sources (aorta and LA), this leads to much greater LV filling; therefore, LV end-diastolic volume increases, which increases LV end-diastolic pressure (20 mmHg in this example). […] Therefore, a defining characteristic of aortic regurgitation is an increase in aortic pulse pressure (systolic minus diastolic pressure). […] The elevation in LV end-diastolic pressure causes blood to back up into the left atrium and pulmonary veins, which increases left atrial pressure and pulmonary capillary wedge pressure, and can cause pulmonary congestion and edema. […] The backward flow of blood into the ventricular chamber during diastole results in a diastolic murmur.
- #1 CV Physiology | Aortic Regurgitationhttps://cvphysiology.com/heart-disease/hd009d
effects of aortic regurgitation on ventricular pressure-volume loopsThe following describes changes that occur in the left ventricular pressure-volume loop when there is aortic regurgitation. In aortic valve regurgitation (red loop in figure), the aortic valve does not close completely at the end of systolic ejection. As the ventricle relaxes during diastole, blood flows from the aorta back into the ventricle, so the ventricle immediately begins to fill from the aorta (before filling from the left atrium). Therefore, there is no true phase of isovolumetric relaxation (no vertical line between aortic valve closure and mitral valve opening) because as the ventricle relaxes, even before the mitral valve opens, blood is entering the ventricle from the aorta, thereby increasing ventricular volume.
- #1 CV Physiology | Aortic Regurgitationhttps://cvphysiology.com/heart-disease/hd009d
Once the mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because aortic pressure is higher than ventricular pressure during diastole. This augments ventricular filling so that end-diastolic volume is increased as shown in the pressure-volume loop. Ventricular end-diastolic volume is also increased because in chronic aortic regurgitation the ventricle anatomically dilates (remodels), which increases ventricular compliance. […] When the ventricle begins to contract and develop pressure, blood is still entering the ventricle from the aorta because aortic pressure is higher than ventricular pressure; therefore, there is no true isovolumetric contraction because volume continues to increase. Once the ventricular pressure exceeds the aortic diastolic pressure, the ventricle ejects blood into the aorta. The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, ventricular peak (systolic) pressure, and stroke volume (as shown by the increased width of the pressure-volume loop).
- #1 Aortic Regurgitation | Thoracic Keyhttps://thoracickey.com/aortic-regurgitation-4/
The majority of causes of aortic regurgitation produce chronic volume overload with slow indolent left ventricular dilation and a prolonged asymptomatic phase. […] In chronic aortic regurgitation excessive preload and excessive afterload may overcome the ability of the left ventricle to compensate via hypertrophy and recruitment of preload reserve, leading to left ventricular systolic dysfunction. This may occur in the absence of symptoms. […] The left ventricle responds to the volume load of chronic AR with a series of compensatory mechanisms, including an increase in end-diastolic volume, an increase in chamber compliance that accommodates the increased volume without a rise in filling pressures, and a combination of eccentric and concentric hypertrophy. […] The central hemodynamic feature of chronic AR is combined volume and pressure overload of the left ventricle.
- #1 Aortic Regurgitation | Thoracic Keyhttps://thoracickey.com/aortic-regurgitation-4/
As the disease progresses, recruitment of preload reserve and compensatory hypertrophy permit the left ventricle to maintain normal ejection performance despite the elevated afterload. […] LV systolic dysfunction (defined as an EF below normal at rest) is initially a reversible phenomenon related predominantly to afterload excess, and full recovery of LV size and function is possible with aortic valve replacement (AVR). […] With time, during which the left ventricle develops progressive chamber enlargement and a more spherical geometry, depressed myocardial contractility predominates over excessive loading as the cause of progressive dysfunction. […] A number of studies have identified LV systolic function and end-systolic size as the most important determinants of survival and postoperative recovery of LV function in patients undergoing valve replacement for chronic AR.
- #1 Aortic regurgitation pathophysiology – wikidochttps://www.wikidoc.org/index.php/Aortic_regurgitation_pathophysiology
Aortic insufficiency causes both volume overload (elevated preload) and pressure overload (elevated afterload due to the increased stroke volume) of the heart. Regurgitation of blood into the left ventricle causes volume overload and a rise in preload. The pressure overload causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. […] The increasing regurgitant volume causes the stroke volume to fall. In order to compensate for a fraction of the blood going backwards, the heart compensates by ejecting a larger total volume of blood forward. The ejection fraction is preserved and perhaps even increased to compensate for the regurgitant fraction. […] While the left ventricular dilation is associated with the increased cardiac output according to the Frank-Starling mechanism, at a certain point of left ventricular dilation, the left ventricle begins to fail as left ventricular contractility falls. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the left ventricle fails. The dramatic enlargement of the heart that is seen with aortic insufficiency is called cor bovinum. […] It has been said that 'aortic regurgitation begets aortic regurgitation’. The high oscillatory shear associated with aortic regurgitation may lead to further dilation of the aorta, which in turn may lead to further worsening of aortic regurgitation.
- #1 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVR – PubMedhttps://pubmed.ncbi.nlm.nih.gov/32529168/
The aim of this review is to describe some of the putative mechanisms implicated in the development of AI, dissect some of the cross-talk among known and possible signaling pathways leading to valve remodeling, identify association between these pathways and pharmacological approaches, and discuss the implications for surgical and percutaneous approaches to AV repair in replacement in the TAVR era.
- #1 Echocardiographic assessment of aortic regurgitation: a narrative review | Echo Research & Practice | Full Texthttps://echo.biomedcentral.com/articles/10.1186/s44156-023-00036-7
Aortic regurgitation (AR) is the third most frequently encountered valve lesion and may be caused by abnormalities of the valve cusps or the aorta. […] Echocardiography is central to the diagnosis and quantification of AR severity, in addition to delineating the aetiology and mechanism of valve insufficiency. […] AR may present and/or develop acutely or gradually and is caused by malcoaptation or malapposition of the AV cusps. […] This may be a result of abnormalities of the AV cusps and/or their supporting structures, including the AV annulus, the aortic root and the ascending aorta. […] Degenerative AV disease is more frequently encountered in the form of focal calcific deposits or diffuse fibrous thickening causing abnormal coaptation, although, rarely, myxomatous degeneration of the aortic cusps may also account for AR secondary to cusp thickening and/or prolapse.
- #1 Echocardiographic assessment of aortic regurgitation: a narrative review | Echo Research & Practice | Full Texthttps://echo.biomedcentral.com/articles/10.1186/s44156-023-00036-7
The functional classification is an invaluable tool that helps clinicians systematically evaluate the valve behaviour and may influence the type of intervention chosen for the valve. […] The VC represents the smallest flow diameter of the regurgitant jet going through the AV, and provides a surrogate for the effective regurgitant orifice area (EROA) and an indicator of the AR severity. […] An EROA0.30cm2, regurgitant volume60mls and regurgitant fraction50% all indicate severe AR. […] In summary, a quantitative assessment of AR should be routinely performed for those patients with more than mild AR. […] Given its significant prognostic value, echocardiographic assessment of the LV is of paramount importance in the evaluation and management of patients with aortic regurgitation not only before but also after they have AV surgery.
- #1 Aortic Regurgitationhttps://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/aortic-regurgitation
This results in increased systolic pressures, reduced diastolic pressures and widened pulse pressure. […] Increased stroke volume leads to a number of unusual peripheral physical examination findings. […] The low diastolic aortic pressures can significantly affect coronary perfusion pressures, as coronary flow occurs during diastole. […] Afterload (peripheral resistance) is an important factor in the degree of aortic regurgitation. […] All other factors being equal, increased peripheral resistance will be associated with increased regurgitation. […] Thus, afterload reduction has become the mainstay of pharmacotherapy in aortic regurgitation.
- #1 Aortic Valve Regurgitation | Cedars-Sinaihttps://www.cedars-sinai.org/health-library/diseases-and-conditions/a/aortic-valve-regurgitation.html
In severe aortic regurgitation, surgery is commonly advised. The timing of surgery is important to discuss with your healthcare provider and surgeon. In some cases, severe aortic regurgitation may be treated with medicine. Medicine may also be used in the short-term before valve replacement surgery. Or it may be used ongoing if you are not able to have valve replacement surgery. […] Acute, severe aortic valve regurgitation needs surgery right away. You may need medicines for a short time to stimulate your heart or to dilate or constrict your blood vessels. In some cases, an infection of the heart valves can cause acute valve regurgitation. This may only need to be treated with antibiotics.
- #1 New minimally invasive treatment option for aortic regurgitation | MUSC Health | Charleston SChttps://muschealth.org/health-professionals/progressnotes/2022/summer/aortic-regurgitation-treatment
Blood flow through the heart is directed through four different valves, each with leaflets, or flaps, that act as one-way doors into the next chamber. But in aortic regurgitation, the aortic valve fails to close completely, and blood leaks backwards through it. […] Patients in South Carolina with severe aortic regurgitation previously had only one treatment option: open heart surgery. But with new transcatheter heart valve technology, a new aortic valve can be placed inside their diseased one by an already established, minimally invasive technique known as transcatheter aortic valve replacement (TAVR). […] This method proved successful for treating aortic stenosis which is when the valve narrows and restricts blood flow but it was not used to treat aortic regurgitation until now. […] With the device, physicians can place a healthy valve inside the leaky one by clipping it onto the natural valves original leaflets without using any sutures.
- #1 New minimally invasive treatment option for aortic regurgitation | MUSC Health | Charleston SChttps://muschealth.org/health-professionals/progressnotes/2022/summer/aortic-regurgitation-treatment
This new device makes TAVR possible for a greater number of patients. […] The device aligns with the patients natural anatomy, he said. This allows for better and more efficient blood flow to the hearts arteries. […] Another drawback to traditional TAVR techniques is coronary re-access, according to Amoroso, but the new valve allows for more successful valve access after placement, which is important for any future procedures. […] I think the procedure offers a treatment opportunity for a whole group of patients whom weve only been able to treat with open heart surgery in the past, he said. This valve offers an alternative for treating patients with aortic regurgitation with a minimally invasive technique that allows patients to recover more quickly.
- #2 Aortic Regurgitation: Background, Pathophysiology, Etiologyhttps://emedicine.medscape.com/article/150490-overview
Aortic regurgitation (AR) is the diastolic flow of blood from the aorta into the left ventricle (LV). Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular apparatus (eg, leaflets, annulus of the aorta) resulting in the diastolic flow of blood into the left ventricular chamber. […] Incompetent closure of the aortic valve can result from intrinsic disease of the leaflets, cusp, diseases of the aorta, or trauma. Diastolic reflux through the aortic valve can lead to left ventricular volume overload. An increase in systolic stroke volume and low diastolic aortic pressure produces an increased pulse pressure. The clinical signs of AR are caused by the forward and backward flow of blood across the aortic valve, leading to increased stroke volume. […] The severity of AR is dependent on the diastolic regurgitant valve area, the diastolic pressure gradient between the aorta and LV, and the duration of diastole.
- #2 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVR – PubMedhttps://pubmed.ncbi.nlm.nih.gov/32529168/
Aortic insufficiency (AI) or regurgitation is caused by the malcoaptation of the aortic valve (AV) cusps due to intrinsic abnormalities of the valve itself, a dilatation or geometric distortion of the aortic root, or by some combination thereof. […] In recent years, there has been an increase in the number of studies suggesting that AI is an active disease process caused by a combination of factors including but not limited to alteration of specific molecular pathways, genetic predisposition, and changes in the mechanotransductive properties of the AV apparatus. […] However, these techniques necessitate frequent reappraisal of the biological and mechanobiological mechanisms underlying AV regurgitation to better understand the risk factors for AI development and recurrence following surgical intervention as well as expand our limited knowledge on patient selection for such procedures.
- #2 Incidence and Pathology of Aortic Regurgitation | ICR Journalhttps://www.icrjournal.com/articles/incidence-and-pathology-aortic-regurgitation?language_content_entity=en
Aortic regurgitation (AR) can arise from degenerative, congenital, inflammatory and infectious aetiologies, manifesting as primary AR with intrinsic leaflet disease, secondary AR due to aortopathy or annular dilatation, or a combination. […] The aetiology of AR may be diverse, encompassing degenerative (degeneration of aortic root and/or aortic leaflet), congenital, inflammatory and infectious factors. The AR mechanism can be primary with aortic valve leaflet abnormality, secondary with preserved aortic leaflets such as aortic root or annular dilatation, or a combination. […] Aortic valve leaflet degeneration is the dominant cause of primary AR. Primary AR consists of calcific degenerative leaflet disease, commonly associated with AS. […] Other causes of primary AR feature intrinsic leaflet disorders such as leaflet perforation, prolapse, or restriction.
- #2 Functional and pathomorphological anatomy of the aortic valve and root for aortic valve sparing surgery in tricuspid and bicuspid aortic valves – Jahanyar- Annals of Cardiothoracic Surgeryhttps://www.annalscts.com/article/view/17021/html
The El Khoury classification thus explains all the different types of AR and illustrates the loss of the geometric relationship between AV-structures. Hence, in analogy to Carpentiers classification: AR type I corresponds to dilation of the FAA; type II corresponds to an excess of leaflet motion (prolapse); and type III to restricted leaflet motion. […] The different mechanisms of AR can be isolated, but they more frequently occur simultaneously in patients with AR especially in cases of long-standing severe AR, large aneurysmal disease or congenital AV disease. […] The goal of AV-sparing surgery and repair is to restore the geometric relationship between the different components of the AV and root, and also to stabilize the repair, which improves long-term durability. Therefore, the surgical toolbox should entail techniques to repair or remodel any component of the AV/root complex; valve-sparing root replacement techniques hereby represent a major tool in the available surgical armamentarium.
- #2 Aortic Valve Regurgitation: Pathophysiology and Implications for Surgical Intervention in the Era of TAVRhttps://pmc.ncbi.nlm.nih.gov/articles/PMC7288848/
The ECM is an important regulator of cell and tissue function and may be defined as the diverse collection of proteins and sugars that surrounds cells in all solid tissues. […] The organized valvular ECM makes up the cusps of the valve and contains three overlapping layers, each with distinct properties: the ventricularis, the spongiosa, and the fibrosa. […] Given the highly interconnected network of proteins and pathways involved in ECM maintenance that have been implicated in AI development, it is safe to suggest that the ECM changes are at the center of the network from which valve remodeling occurs. […] Cardiac remodeling resulting in AI can manifest itself in various ways, such as prolapse, degeneration, and calcification, which can result in changes in the hemodynamic properties of the valve. […] The rise of proteomics and knockout studies on individual proteins in mice over recent years has demonstrated that numerous different proteins can contribute to AV remodeling and AI when inactivated.
- #2 Aortic Regurgitation – Cardiovascular Disorders – Merck Manual Professional Editionhttps://www.merckmanuals.com/professional/cardiovascular-disorders/valvular-disorders/aortic-regurgitation
Aortic regurgitation (AR) is incompetency of the aortic valve causing backflow from the aorta into the left ventricle during diastole. […] Aortic regurgitation may be acute (very uncommonly) or chronic. […] In aortic regurgitation, volume overload of the left ventricle (LV) occurs because the LV receives blood regurgitated from the aorta during diastole in addition to blood from the left atrium. […] In acute aortic regurgitation, the LV does not have time to dilate to accommodate the increased volume, which then causes a rapid increase in left ventricular pressure and subsequently pulmonary edema and decreased cardiac output. […] In chronic aortic regurgitation, LV hypertrophy and dilation can gradually occur, so normal left ventricular pressures and cardiac output are maintained. But decompensation eventually develops, ultimately causing arrhythmias, LV impairment, and heart failure (HF).
- #2 Acute aortic regurgitation in adults – UpToDatehttps://www.uptodate.com/contents/acute-aortic-regurgitation-in-adults
The acute onset of severe aortic regurgitation (AR, also called aortic insufficiency) is usually a medical emergency due to the inability of the left ventricle to quickly adapt to the abrupt increase in end-diastolic volume caused by the regurgitant flow. If not surgically corrected, acute severe AR commonly results in cardiogenic shock. […] Aortic dissection can result in AR by four mechanisms: dilation of the sinuses with incomplete coaptation of the leaflets at the center of the valve; involvement of a valve commissure resulting in inadequate leaflet support; direct extension of the dissection into the base of a leaflet, resulting in a flail valve leaflet; and prolapse of the dissection flap across the aortic valve into the left ventricular outflow tract in diastole impeding leaflet closure. Patients with a bicuspid aortic valve are at higher risk of aortic dissection.
- #2 Chronic aortic regurgitation: diagnosis and therapy in the modern erahttps://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/chronic-aortic-regurgitation-diagnosis-and-therapy-in-the-modern-era
In fixed subaortic stenosis, which is usually classified as a congenital lesion, the incessant high-pressure jet may damage the aortic leaflets. Therefore, some degree of AR is frequently incurred in a progressive manner dependent on the severity of obstruction. […] Chronic AR generally evolves slowly and imposes a combined volume (manifested by LV enlargement) and pressure overload (indicated by increased end-systolic pressure) on the LV. This hybrid haemodynamic overload results in remodelling of the LV to normalise wall stress and maintain systolic function and is characterised by eccentric hypertrophy and LV dilatation to accommodate for the regurgitant volume. […] The onset of symptoms (spontaneous or on exercise testing) represents a key development and denotes the strongest indication for intervention.
- #2 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #2 Aortic regurgitation pathophysiology – wikidochttps://www.wikidoc.org/index.php/Aortic_regurgitation_pathophysiology
Aortic insufficiency causes both volume overload (elevated preload) and pressure overload (elevated afterload due to the increased stroke volume) of the heart. Regurgitation of blood into the left ventricle causes volume overload and a rise in preload. The pressure overload causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. […] The increasing regurgitant volume causes the stroke volume to fall. In order to compensate for a fraction of the blood going backwards, the heart compensates by ejecting a larger total volume of blood forward. The ejection fraction is preserved and perhaps even increased to compensate for the regurgitant fraction. […] While the left ventricular dilation is associated with the increased cardiac output according to the Frank-Starling mechanism, at a certain point of left ventricular dilation, the left ventricle begins to fail as left ventricular contractility falls. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the left ventricle fails. The dramatic enlargement of the heart that is seen with aortic insufficiency is called cor bovinum. […] It has been said that 'aortic regurgitation begets aortic regurgitation’. The high oscillatory shear associated with aortic regurgitation may lead to further dilation of the aorta, which in turn may lead to further worsening of aortic regurgitation.
- #2 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #2 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #2 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #2 Aortic Regurgitation – Aortic Valve Disease – Valvular Heart Disease – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicinehttps://empendium.com/mcmtextbook/chapter/B31.II.2.8.2.
Aortic regurgitation (AR) is a reversal of blood flow from the aorta into the left ventricle (LV) due to incomplete closure of the aortic valve leaflets. […] Primary regurgitation is caused by damage to or a congenital abnormality of the leaflets, with subsequent dilation of the left ventricular outflow tract, aortic annulus, and ascending aorta. […] Secondary regurgitation is caused by dilation of the aortic annulus and the ascending aorta (secondarily causing malcoaptation of the aortic valve leaflets) in the absence of significant aortic valve leaflet pathology. […] 1) Primary: Congenital (bicuspid aortic valve, quadricuspid aortic valve, valve damage in subaortic stenosis); degenerative (calcifications, fibrosis); infective endocarditis (active or healed); rheumatic; drug-induced (fenfluramine, phentermine) damage of the leaflets.
- #2 Incidence and Pathology of Aortic Regurgitation | ICR Journalhttps://www.icrjournal.com/articles/incidence-and-pathology-aortic-regurgitation?language_content_entity=en
In secondary AR, the aortic valve leaflets appear structurally normal. Aortic root pathology with dilatation can create secondary AR through aortic valve leaflet malcoaptation, retraction and prolapse. […] The bicuspid aortic valve phenotype is the most common congenital heart defect, and associated with AR in 20-70% of cases. […] Primary AR can develop due to abnormal shear stress leading to degenerative leaflet thickening, restriction, or prolapse. […] Connective tissue disorders such as Marfan, Loeys-Dietz and vascular Ehlers-Danlos syndromes commonly result in secondary AR due to aortopathy. […] The main cause of acute secondary AR is aortic dissection, which may be iatrogenic or due to the above-mentioned aortopathies. […] In acute AR, the sudden onset of severe diastolic regurgitation results in a rapid increase in LV end diastolic volume and pressure, which may spiral towards pulmonary congestion and cardiogenic shock. In chronic AR, the left ventricle has the time to adapt to the volume overload and the LV end diastolic pressure volume relationship flattens, which postpones the occurrence of symptoms. Remodelling includes LV dilatation, eccentric hypertrophy and increased stroke volume to compensate for the regurgitation volume. However, over time the incessant volume overload will overrule the ventricular compensatory remodelling capacity. Eventually, this cascade will progress to LV dilatation, myocardial fibrosis and systolic failure with depressed LVEF.
- #2 Aortic Regurgitation – Aortic Valve Disease – Valvular Heart Disease – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicinehttps://empendium.com/mcmtextbook/chapter/B31.II.2.8.2.
2) Secondary: Idiopathic aortic dilation; hypertensive aortic dilation; systemic connective tissue diseases (rheumatic disease, rheumatoid arthritis, aortic stenosis); dilation or dissection of the ascending aorta (hypertension, Marfan or Marfan-like syndrome, atherosclerosis, inflammation, trauma, myxomatous degeneration); aortopathy associated with bicuspid aortic valve; syphilitic aortic disease.
- #2 Aortic Regurgitation: Symptoms, Causes & Treatmenthttps://my.clevelandclinic.org/health/diseases/24396-aortic-regurgitation
Over time, this can cause the muscular walls of your left ventricle to thicken and dilate (left ventricular hypertrophy). This makes your heart less efficient. Other complications may include heart failure and arrhythmia. […] Acute aortic regurgitation can cause pulmonary edema (fluid in your lungs) and lower your cardiac output.
- #2 CV Physiology | Aortic Regurgitationhttps://cvphysiology.com/heart-disease/hd009d
Once the mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because aortic pressure is higher than ventricular pressure during diastole. This augments ventricular filling so that end-diastolic volume is increased as shown in the pressure-volume loop. Ventricular end-diastolic volume is also increased because in chronic aortic regurgitation the ventricle anatomically dilates (remodels), which increases ventricular compliance. […] When the ventricle begins to contract and develop pressure, blood is still entering the ventricle from the aorta because aortic pressure is higher than ventricular pressure; therefore, there is no true isovolumetric contraction because volume continues to increase. Once the ventricular pressure exceeds the aortic diastolic pressure, the ventricle ejects blood into the aorta. The increased end-diastolic volume (increased preload) activates the Frank-Starling mechanism to increase the force of contraction, ventricular peak (systolic) pressure, and stroke volume (as shown by the increased width of the pressure-volume loop).
- #2 6.5: Aortic Regurgitation – Medicine LibreTextshttps://med.libretexts.org/Bookshelves/Medicine/Textbook_of_Cardiology/06%3A_Valvular_Disease/6.05%3A_Aortic_Regurgitation
Aortic root dilatation, annular dilation and congenital bicuspid valve are, in developed countries, the most common causes of severe chronic aortic valve regurgitation. […] The slow process of chronic aortic regurgitation allows adaptation of the ventricle to the increased preload and afterload. […] The left ventricle compensates to the regurgitant flow, the increased volume and pressure by enlargement. […] In contrast to the compensatory mechanism in mitral valve regurgitation, a modest concentric left ventricular hypertrophy accompanies the eccentric hypertrophy, with a normal mass-to-volume ratio. […] In a chronic state, progressive left ventricle dilatation leads to pre- and afterload mismatch.
- #3 Echocardiographic assessment of aortic regurgitation: a practical guideline from the British Society of Echocardiography | Echo Research & Practice | Full Texthttps://echo.biomedcentral.com/articles/10.1186/s44156-024-00067-8
Aortic regurgitation (AR) is the result of aortic cusp abnormality, aortic root (AoR) dilatation, or a combination of the two. […] It is useful to classify the mechanism of valve insufficiency into one of three subtypes: Type I AR is characterised by normal cusp motion within the context of aortic dilatation or cusp perforation; Type II describes excessive motion such as cusp prolapse; and Type III is the consequence of cusp restriction. […] The functional classification is a useful tool that helps clinicians systematically evaluate the valve behaviour and may influence the type of intervention chosen for the valve. However when reporting, it may be necessary to describe the mechanism rather than just quote the functional classification type. This would ensure findings are effectively communicated, relatable and transferable across echocardiographer, referrer and receiver (i.e. normal cusp motion in the setting of a dilated aorta).
- #3 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303
- #3 Aortic Regurgitation – Aortic Valve Disease – Valvular Heart Disease – Cardiovascular Diseases – Diseases – McMaster Textbook of Internal Medicinehttps://empendium.com/mcmtextbook/chapter/B31.II.2.8.2.
Aortic regurgitation (AR) is a reversal of blood flow from the aorta into the left ventricle (LV) due to incomplete closure of the aortic valve leaflets. […] Primary regurgitation is caused by damage to or a congenital abnormality of the leaflets, with subsequent dilation of the left ventricular outflow tract, aortic annulus, and ascending aorta. […] Secondary regurgitation is caused by dilation of the aortic annulus and the ascending aorta (secondarily causing malcoaptation of the aortic valve leaflets) in the absence of significant aortic valve leaflet pathology. […] 1) Primary: Congenital (bicuspid aortic valve, quadricuspid aortic valve, valve damage in subaortic stenosis); degenerative (calcifications, fibrosis); infective endocarditis (active or healed); rheumatic; drug-induced (fenfluramine, phentermine) damage of the leaflets.
- #4 Pathophysiology of aortic regurgitation and management | PPThttps://www.slideshare.net/slideshow/pathophysiology-of-aortic-regurgitation-and-management-129052303/129052303